Poster Presentation ESA-SRB-ANZOS 2025 in conjunction with ENSA

Do all good things come in pairs? An atypical case of bilateral adrenal masses with cosecretion (128762)

Yuhan Goh 1 , Ee Mun Lim 2 3 , Gregory Ong 4 , Kyaw Thura 5
  1. Diabetes and Endocrinology, Royal Perth Hospital, Perth, Western Australia, Australia
  2. Endocrinology and Diabetes, Sir Charles Gairdner Hospital, Nedlands, Western Australia, Australia
  3. Department of Clinical Biochemistry, Sir Charles Gairdner Hospital, Nedlands, Western Australia, Australia
  4. Department of Endocrinology and Diabetes, Fiona Stanley Hospital, Murdoch, Western Australia, Australia
  5. Department of Endocrinology and Diabetes, Rockingham General Hospital, Cooloongup, Western Australia, Australia

Case summary: A 50-year-old male with a background of familial adenomatous polyposis (FAP), colectomy and loop ileostomy 2002 with high stoma output, presented with large bilateral adrenal lesions (right 57mm, left 59mm) with benign characteristics on CT in 2024(figure 1). Lesions were absent in 2006 and present on CT 2022 (10mm smaller). Malignancy could not be excluded on FDG-PET/CT(figure 2)

Cosecretion of aldosterone and cortisol was confirmed(table 1). Plasma aldosterone was markedly elevated (50,700, 136,000pmol/L) by immunoassay and confirmed by LCMS(table 1), with unsuppressed renin, elevated ARR and unremarkable sodium and potassium(table 1). An LCMS 18-analyte-steroid-panel measured on a stored serum sample from 2009 demonstrated an isolated elevated aldosterone 7,710pmol/L (an order of magnitude less to 2024)(table 2). The same assay in 2024 demonstrated elevated aldosterone precursors 11-deoxycorticosterone and corticosterone(figure 3). ACTH was undetectable, presumedly suppressed by adrenal metabolites. He had no clinical manifestations of primary aldosteronism or Cushing’s syndrome (besides obesity). Plasma metanephrines were unremarkable

His markedly elevated aldosterone with unsuppressed renin were considered a homeostatic response to decades of unattended high stoma output i.e. longstanding compensatory secondary aldosteronism(1). This process, with his genetic predisposition(2), presumedly lead to the development of large bilateral adenomas and increased secretion of aldosterone precursors. Aldosterone resistance via downregulation of (or defective) intestinal mineralocorticoid receptor (MR) and epithelial sodium channels (ENaC) may be contributory(3,4). MACS was present which is associated with bilateral lesions (5). He was referred to the stoma nurse and is undergoing surveillance for malignant transformation and clinical features of MACS.

Discussion: The physiology of mucosal adaptation and sodium resorption post bowel surgery, mediated by hyperaldosteronism and upregulation of ENaC, will be outlined(1,6,7). Aldosterone resistance in the context of excessive gastrointestinal fluid loss will be explored(3,4). Finally, the associations between FAP and adrenal masses, malignancy and hormone excess will be reviewed(2,8,9,10).

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